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The Journal of Neuroscience, December 10, 2003, 23(36):11382-11391

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Development/Plasticity/Repair
Plasticity of GABAB Receptor-Mediated Heterosynaptic Interactions at Mossy Fibers After Status Epilepticus

Kate E. Chandler,1 Alessandra P. Princivalle,2 Ruth Fabian-Fine,3 Norman G. Bowery,2 Dimitri M. Kullmann,1 and Matthew C. Walker1

1Institute of Neurology, University College London, London WC1N 3BG, United Kingdom, 2Department of Pharmacology, University of Birmingham, Birmingham B15 2TT, United Kingdom, and 3Department of Psychology and Neuroscience Institute, Dalhousie University, Halifax, Nova Scotia B3H 4J1, Canada

Several neurotransmitters, including GABA acting at presynaptic GABAB receptors, modulate glutamate release at synapses between hippocampal mossy fibers and CA3 pyramidal neurons. This phenomenon gates excitation of the hippocampus and may therefore prevent limbic seizure propagation. Here we report that status epilepticus, triggered by either perforant path stimulation or pilocarpine administration, was followed 24 hr later by a loss of GABAB receptor-mediated heterosynaptic depression among populations of mossy fibers. This was accompanied by a decrease in the sensitivity of mossy fiber transmission to the exogenous GABAB receptor agonist baclofen. Autoradiography revealed a reduction in GABAB receptor binding in the stratum lucidum after status epilepticus. Failure of GABAB receptor-mediated modulation of mossy fiber transmission at mossy fibers may contribute to the development of spontaneous seizures after status epilepticus.

Key words: epilepsy; GABAB receptor; status epilepticus; mossy fibers; CA3; seizures

Received May 21, 2003; revised September 22, 2003; accepted September 24, 2003.






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